Arteriosclerosis, Thrombosis, and Vascular Biology. 1995;15:320-324
© 1995 American Heart Association, Inc.
Articles |
Relation Between Insulin Resistance, Hyperinsulinemia, Postheparin Plasma Lipoprotein Lipase Activity, and Postprandial Lipemia
From the Department of Medicine, Stanford University School of Medicine, and the Geriatric Research, Education and Clinical Center, Department of Veterans Affairs Medical Center, Palo Alto, Calif.
Correspondence to Gerald Reaven, Geriatric Research, Education and Clinical Center, Department of Veterans Affairs Medical Center, 3801 Miranda Ave (182-B), Palo Alto, CA 94304.
Abstract We examined the relation between insulin resistance, plasma glucose and insulin responses to meals, lipoprotein lipase (LPL) activity, and postprandial lipemia in a population of 37 healthy nondiabetic individuals. Plasma glucose and insulin concentrations were determined at frequent intervals from 8 AM through midnight (breakfast at 8 AM and lunch at noon); resistance to insulin-mediated glucose disposal was determined by measuring the steady-state plasma glucose (SSPG) concentration at the end of a 180-minute infusion of glucose, insulin, and somatostatin; LPL activity was quantified in postheparin plasma; and postprandial concentrations of triglyceride (TG)-rich lipoproteins were assessed by measuring the TG and retinyl palmitate content in plasma and the Svedberg flotation index (Sf) >400 and Sf 20 to 400 lipoprotein fractions. Significant simple correlation coefficients were found between various estimates of postprandial lipemia and SSPG (r=.38 to .68), daylong insulin response (r=.37 to .58), daylong glucose response (r=.10 to .39), and LPL activity (r=-.08 to -.58). However, when multiple regression analysis was performed, only SSPG remained independently associated with both postprandial TG and retinyl palmitate concentrations. These data provide evidence that insulin resistance plays an important role in regulating the postprandial concentration of TG-rich lipoproteins, including those of intestinal origin.
Key Words: insulin resistance • hyperinsulinemia • intestinal lipoproteins • postheparin lipoprotein lipase activity • postprandial lipemia
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